Mammalian ATG8 proteins (mATG8s), including LC3 and GABARAP families, are crucial for autophagosome biogenesis and cargo recruitment during autophagy. This process is tightly regulated by many mATG8-associated proteins with LC3 interacting regions (LIR). Although many LIR-containing proteins have been identified, their specific physiological relevance in modulating mice behavior is largely unknown. Therefore, in this study, to elucidate potential roles of LIR-mediated mATG8 function in mice behavior, we have generated knock-in mice overexpressing HyD-LIR(TP)-Venus which specifically binds to mATG8s (LC3s, or GABARAPs) using CaMKII-CRE-inducible system known to exhibit selectivity for excitatory glutamatergic neurons in vivo. Indeed, HyD-LIR(TP)-Venus was localized predominantly to LC3 family or GABARAP family-positive autophagosomes in the hippocampal or cortical neurons, leading to an accumulation of p62, a selective autophagy substrate, especially in the hippocampus and cortex but not in the cerebellum. This suggests an impairment in autophagic flux through the sequestration of endogenous LC3s and GABARAPs. To investigate the effect of LIR-mediated mATG8 by HyD-LIR(TP)-Venus on learning and memory, we performed behavioral tests including object location memory, three-chamber, and Morris water-maze tests. Very interestingly, the expression of HyD-LIR(TP)-Venus in excitatory glutamatergic neurons resulted in deficits in object location memory, social recognition memory, without affecting anxiety levels or spatial memory in the Morris water maze test. Proteomic analysis identified several synaptic proteins with LIR motifs as potential mediators of social memory deficits in mice, highlighting the critical role of LIR-containing proteins in neuronal autophagy and cognitive behaviors. This study reveals novel insights into how mATG8s and their interactions with LIR-containing synaptic proteins influence neuronal autophagy and social recognition memory.